Naringenin Inhibits Glucose Uptake in MCF-7 Breast Cancer Cells: A Mechanism for Impaired Cellular Proliferation

  title={Naringenin Inhibits Glucose Uptake in MCF-7 Breast Cancer Cells: A Mechanism for Impaired Cellular Proliferation},
  author={Anne W. Harmon and Yashomati M. Patel},
  journal={Breast Cancer Research and Treatment},
  • A. W. Harmon, Y. Patel
  • Published 1 May 2004
  • Biology, Medicine, Chemistry
  • Breast Cancer Research and Treatment
Certain flavonoids inhibit glucose uptake in cultured cells. In this report, we show that the grapefruit flavanone naringenin inhibited insulin-stimulated glucose uptake in proliferating and growth-arrested MCF-7 breast cancer cells. Our findings indicate that naringenin inhibits the activity of phosphoinositide 3-kinase (PI3K), a key regulator of insulin-induced GLUT4 translocation, as shown by impaired phosphorylation of the downstream signaling molecule Akt. Naringenin also inhibited the… 
Cytotoxic effects of 7-O-butyl naringenin on human breast cancer MCF-7 cells
The results indicate that the BN-induced cytotoxicity of MCF-7 cells is mediated by the generation of ROS as well as through the p38, SAPK/JNK1/2, and c-Jun activation signaling pathways, and may therefore possess chemotherapeutic potential as an anti-proliferative agent.
Genistein induces glucose-regulated protein 78 in mammary tumor cells.
The results suggest that genistein may be exploited as an enhancer of chemotherapeutic agents in certain types of breast cancer.
17β-estradiol activates glucose uptake via GLUT4 translocation and PI3K/Akt signaling pathway in MCF-7 cells.
An ER-dependent activation of some of the key steps of the PI3K/Akt signaling pathway cascade that leads cells to improve some mechanisms that finally increase glucose uptake capacity is reported.
Antimetabolic Effects of Polyphenols in Breast Cancer Cells: Focus on Glucose Uptake and Metabolism
This work will review data showing an antimetabolic effect of polyphenols and its involvement in the chemopreventive/chemotherapeutic potential of these dietary compounds, in relation to breast cancer.
Regulation of GLUT transporters by flavonoids in androgen-sensitive and -insensitive prostate cancer cells.
P phenotypic characteristics of prostate cancer cells are responsible for the different effects of these flavonoids in glucose uptake and in GLUT expression rather than their structural differences, with the most effective in reducing cell growth being the highest in modifying glucose absorption and GLUT levels.
Naringenin Inhibits Proliferation and Survival of Tamoxifen‐ Resistant Breast Cancer Cells
It is shown that Nar impairs cell proliferation and induces apoptosis of Tam‐R MCF‐7 breast cancer cells, and the flavanone Naringenin (Nar) is identified as an inhibitor of both the PI3K and MAPK pathways.
Naringenin and falcarinol stimulate glucose uptake and TBC1D1 phosphorylation in porcine myotube cultures
It is shown that naringenin and falcarinol enhance phosphorylation of TBC1D1 suggesting that these compounds enhance translocation of Glut4 containing vesicles and thereby GU via a TBC 1D1-dependent mechanism.
Ifosfamide metabolite chloroacetaldehyde inhibits cell proliferation and glucose metabolism without decreasing cellular ATP content in human breast cancer cells MCF‐7
The results show that low CAA concentrations inhibited cell proliferation in a concentration‐dependent manner and suggests that it might play a role in the antitumor activity of IFO.


Naringenin inhibits phosphoinositide 3-kinase activity and glucose uptake in 3T3-L1 adipocytes.
Flavonoids are potential inhibitors of glucose uptake in U937 cells.
  • J. B. Park
  • Biology
    Biochemical and biophysical research communications
  • 1999
It is shown that some types of natural flavonoids block glucose uptake in myelocytic U937 cells and that natural Flavonoids could be used as alternative blockers of glucose uptake at the concentrations of 8-50 microM in vitro.
Mitogen-activated Protein Kinase Kinase Inhibition Does Not Block the Stimulation of Glucose Utilization by Insulin (*)
The results indicate that stimulation of the MAPK pathway by insulin is not required for many of the metabolic activities of the hormone in cultured fat and muscle cells.
Glucose transporters and transport kinetics in retinoic acid-differentiated T47D human breast cancer cells.
In conclusion, differentiation of human breast cancer cells appears to be associated with decreased glycolysis by a mechanism that involves a reduction in GLUT-1 and a slowdown of glucose transport.
A synthetic inhibitor of the mitogen-activated protein kinase cascade.
Results indicate that the MAPK pathway is essential for growth and maintenance of the ras-transformed phenotype and PD 098059 is an invaluable tool that will help elucidate the role of theMAPK cascade in a variety of biological settings.
The mitogen-activated protein kinase pathway can mediate growth inhibition and proliferation in smooth muscle cells. Dependence on the availability of downstream targets.
The MAPK pathway mediates either proliferation or growth inhibition in human arterial SMCs depending on the availability of specific downstream enzyme targets.
Inhibition of human breast cancer cell proliferation and delay of mammary tumorigenesis by flavonoids and citrus juices.
Evidence of anticancer properties of orange juice and indicate that citrus flavonoids are effective inhibitors of human breast cancer cell proliferation in vitro are provided, especially when paired with quercetin, which is widely distributed in other foods.
A shift from normal to high glucose levels stimulates cell proliferation in drug sensitive MCF‐7 human breast cancer cells but not in multidrug resistant MCF‐7/ADR cells which overproduce PKC‐βII
A link between high glucose‐induced PKC‐βII isozyme down‐regulation with concomitant acceleration of cell cycle progression in MCF‐7 cells is demonstrated.